Staphylococcus epidermidis is a frequent cause of nosocomial infections. The central virulence factor of S. epidermidis is biofilm formation. Polysaccharide intercellular adhesin (PIA) constitutes the major biofilm matrix-component. PIA and biofilm have been implicated in S. epidermidis evasion of host immune defence. We examined the effects of S. epidermidis PIA on the inflammatory response with focus on complement activation. We used a human whole-blood ex vivo model of infection and compared the effects of a PIA-positive S. epidermidis strain (SE1457) and its PIA-negative isogenic mutant (M10). The independent effect of purified PIA on complement activation was investigated. In glucose-rich media, the mutant formed a proteinacious DNA-rich biofilm, whereas SE1457 formed a thick PIA-biofilm. In biofilm growth, SE1457 induced a stronger activation of the complement system compared with M10. We verified that purified PIA was independently responsible for a strong activation of the complement system. In contrast, M10 induced higher granulocyte activation by expression of CD11b and higher secretion of cytokines. We conclude that PIA has potent pro-inflammatory properties by activating the complement system. However, in a complex balance of the immune response, the decreased activation of granulocytes and cytokines by a PIA biofilm may limit host eradication of S. epidermidis.
ABSTRACT:The arginine catabolic mobile element (ACME) in Staphylococci encodes several putative virulence factors. ACME appears to have been transferred from Staphylococcus epidermidis into Staphylococcus aureus and is strongly associated with the epidemic and virulent S. aureus USA300. We sought to determine the distribution of ACME in 128 S. epidermidis blood culture isolates from neonates and to assess ACME's impact on antibiotic resistance, biofilm production, invasive capacity, and host inflammatory response. ACME was detected in 15/64 (23%) invasive blood culture isolates and 26/64 (40%) blood culture contaminants (p ϭ 0.02). ACME-positive S. epidermidis isolates displayed less antibiotic resistance (p Ͻ 0.001) and were collected from more mature neonates (p ϭ 0.001). Biofilm production was more prevalent among ACMEnegative isolates (61/87) compared with ACME positive (18/41; p ϭ 0.004). Among the 64 children considered having an invasive infection, ACME did not influence the maximum C-reactive protein level. In an in vitro whole-blood sepsis model, there were no differences in the inflammatory response between ACME-positive and ACMEnegative isolates. We conclude that ACME in S. epidermidis from neonates was associated with less antibiotic resistance and also does not seem to be associated with increased pathogenicity. (Pediatr Res 68: 237-241, 2010) S taphylococcus epidermidis is a frequent cause of late onset sepsis in preterm neonates (1,2). The major virulence factor of S. epidermidis is biofilm formation on polymer surfaces, i.e. indwelling central venous lines (3). A wide range of other putative virulence factors, e.g. surface proteins (4), phenol soluble modulins (PSM), and poly-␥-glutamic acid (3,5-7), have also been identified. However, their clinical relevance is yet to be proven.The arginine catabolic mobile element (ACME) is a genomic island in Staphylococci that may contribute to enhanced pathogenicity. It was first discovered in the community associated methicillin-resistant Staphylococcus aureus (CA-MRSA) USA300 strain and the biofilm-negative S. epidermidis strain ATCC12228 (8). ACME contains two characteristic gene clusters (the arc-operon and the opp3-operon) that are homologs of virulence determinants in other bacterial species. The arc-operon, a characteristic cluster of six genes, encodes several enzymes in the arginine deiminase catabolic pathway, a putative virulence pathway that convert L-arginine to carbon dioxide, carbamoyl ornithine, ammonia, and ATP (9,10). The opp3-operon encodes an oligopeptide permease system. Similar opp-operons in other bacterial species have a wide array of functions including pheromone transport, chemotaxis, and expression of virulence determinants (8). ACME has been divided into three allotypes (8 -11). ACME-I, first found in S. aureus USA300, possess the arc-operon and the opp3-operon. ACME-II, first found in S. epidermidis ATCC12228, consists mainly of the arc-operon. ACME-III has only the opp3-operon and lacks the arc-operon. All three allotypes have ...
Treatment with vancomycin or Ltx21 was not sufficient to achieve complete bacterial clearance of implants, underlining the difficulties of treating such infections. The low-grade infection may attenuate the inflammatory response and contribute to impaired bacterial clearance.
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